In reference to Otoconia and Otolithic Membrane Fragments Within the Posterior Semicircular Canal in Benign Paroxysmal Positional Vertigo

We certainly enjoyed the article “Otoconia and Otolithic Membrane Fragments Within the Posterior Semicircular Canal in Benign Paroxysmal Positional Vertigo” by Kao et al. in the March 2017 issue of The Laryngoscope. The authors found otoconia, along with fragments of the otolithic membrane, displaced from the utricle en bloc and present in the posterior canal. This coincides with our theory that many labyrinthine injuries may involve elevation of this membrane from the neurosensory endings of the utricle and saccule. Separate from the positioning vertigo that occurs after these fragments detached and became dislodged within the semicircular canal, these patients experience a sensation of imbalance or equilibrium disturbances at rest. We hypothesize this is caused by modulation and dysfunction of the normal continuous tonic resting firing rate of hair cells of the vestibular nerve imbedded in the otolithic organs. Initial damage to the otolithic organ may occur from previously described predisposing factors to benign paroxysmal positional vertigo (BPPV) such as vascular ischemia, inflammation, and trauma. This allows for incipient damage with secondary elevation of the neuroepithelial layer in a process similar to retinal detachment of the eye. Patients then may or may not go on to develop classic BPPV, depending on whether the elevation becomes fully detached. This explains both patients who develop disequilibrium despite normal caloric and positioning testing and patients who previously had BPPV and still complain of disequilibrium despite the absence of positioning rotary nystagmus. Further study of this issue is warranted, and I applaud the authors on their work on this important condition.